CSB Faculty

Qitao Ran, Ph.D.

The main interest of my lab is to investigate the roles of mitochondrial dysfunction and oxidative stress in the pathogenesis of neurodegenerative diseases such as Alzheimer's disease and brain aging. The ultimate goal of my research is to identify new therapeutic targets for neurodegenerative diseases and brain aging.

Antioxidant defense enzymes, such as glutathione peroxidase 4 (Gpx4), peroxiredoxin 3 (Prdx3), glutaredoxin 2 (Glrx2), are essential for protecting mitochondria from damage induced by reactive oxygen species. My lab has generated a series of transgenic and knockout mouse models that under- or over- express these antioxidant defense enzymes. By studying brain dysfunction and pathologies associated with Alzheimer's disease in these animals, we can decipher mechanistic contributions of mitochondrial oxidative stress in disease pathogenesis. For example, we showed that knockout of Gpx4, an antioxidant defense enzyme important in protecting mitochondrial membranes from oxidative damage, causes neurodegeneration in brain. And we showed that mitochondria H2O2 plays a key role in cognitive impairment and Aβ accumulation in brain using Prdx3 transgenic mice. Using whole animals as well as cultured cells from the mice, we are investigating the specific roles of mitochondrial oxidative stress on neural injury and cognition impairment.

I am also interested in understanding the role of toxin exposure in Alzheimer's disease pathogenesis, because emerging epidemiological data indicate that exposure to environmental toxins may elevate the risk of Alzheimer's disease. Using Alzheimer's disease mouse models and animal models generated in my lab, we are studying how toxin exposure may lead to decreased cognition and overproduction of Aβ.